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• W2000587413 abstract "Reduction of transient outward current (Ito) and excessive activation of Ca2+/Calmodulin-dependent kinase II (CaMKII) are general features of ventricular myocytes in heart failure. We hypothesize that alterations of Ito directly regulate CaMKII activation in cardiomyocytes. A dynamic coupling of Ito channel subunit Kv4.3 and inactive CaMKII was discovered in cardiomyocytes with the membrane predominant distribution by co-immunoprecipitation and fluorescence resonance energy transfer techniques. CaMKII dissociation from Kv4.3–CaMKII units caused a significant increase in CaMKII autophosphorylation and L-type calcium current (ICa) facilitation. ICa facilitation was blunted by the compartmental Ca2+ chelator BAPTA but unaffected by bulk Ca2+ chelator EGTA, implicating membrane-localized CaMKII. Kv4.3 overexpression reduced basal CaMKII autophosphorylation in myocytes and eliminated Ca2+-induced CaMKII activation. Kv4.3 blocks CaMKII activation by binding to the calmodulin binding sites, whereas Kv4.3 uncoupling releases these sites and leads to a substantial CaMKII activation. Our results uncovered an important mechanism that regulates CaMKII activation in the heart and implicate Ito channel alteration in pathological CaMKII activation." @default.
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• W2000587413 date "2010-12-08" @default.
• W2000587413 modified "2023-09-23" @default.
• W2000587413 title "Dynamic Kv4.3–CaMKII unit in heart: an intrinsic negative regulator for CaMKII activation" @default.
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• W2000587413 doi "https://doi.org/10.1093/eurheartj/ehq469" @default.
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